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By virtue of my specialization in pediatric ophthalmology, strabismus and neuro-ophthalmology, I get to see a large number of children with mental retardation and visual impairment In my clinic. In a lot of such situations, this is their first visit to an ophthalmologist as the parents have been busy with managing the developmental delay and have been visiting the paediatrician. It is generally when a paediatrician or paediatric neurologist sees them and refers them to me that the parents begin to realise there is something wrong with the child’s eyes. In a contrast to this presentation, there are cases where the parents notice that the child does not seem to be making eye contact with them or seems disinterested in his/her surroundings or has an obvious eye abnormality such as squint (misaligned eyes) or cataract (white reflex in the eyes), and bring the child to me first. It is on examination that I realise there is a generalised developmental delay and the problem encompasses a lot more than an eye disease alone. These cases are then referred to the paediatric neurologist who evaluates the child in detail. Either way, both cases require a comprehensive multi-disciplinary management strategy and are a challenge for rehabilitation therapists and physicians. In this article, I will briefly touch upon the ophthalmologists’ perspective to visual rehabilitation of a child with mental retardation through the help of a case I had recently encountered in my clinic.

A 14 month old boy was referred to me by my paediatric neurologist colleague with history of hypoxia at birth resulting in generalised developmental delay. The child was born to a non-consanguineous marriage and had a relatively uneventful antenatal life in the mother’s womb. The mother was a young primipara in her early twenties and lived in Gwalior, India. She was taken up for a induced vaginal delivery at a nursing home in her town as she had reached full term. Unfortunately during the induction, a prolonged labour ensued and there was fetal distress with meconium stained liquor. Since the nursing home did not have adequate facility for an emergency caesarean section at the time, the delivery was completed with assistance of forceps. The child did not cry at birth and was noted to be cyanosed though there was no written record documenting this. The history I took from the child’s family clearly pointed towards a limp, lifeless baby who needed to be resuscitated and began to cry after a few minutes of birth. After the delivery, everything seemed uneventful and the child was feeding well though less interactive. It was around 6 months of age that the family started to note that the child was “slow” and could not hold the neck or fixate at any object. The eyes seemed to dance around but they thought this would get better and their paediatrician asked them to wait for some more time. By the time the child was 1 year old, he could hold his head but could barely sit with support but not without it and could vocalise with sounds but no words. The child’s eyes would still dance around and the child could not fixate at either the mother’s face or any object. Some jerky head movements were also noted but seizures were ruled out. The child was then seen by a pediatric neurologist who advised an MRI and found gliotic changes in the brain and diagnosed it as a case of generalised development delay secondary to hypoxic ischemic encephalopathy. The child was also sent for an ENT exam where the BERA test was normal (indicating a normal hearing). The child was also sent to me for an ophthalmic evaluation.

I examined the child when the child was fully awake and alert and found that the child could perceive light from my torch but could not fixate or follow it. There was a nystagmus (wriggly dancing eye movements) in both eyes. I tried testing the vision of the child with the use of special charts called Lea gratings but the child seemed to be unable to fixate at them. I understood that the child has a poor vision and I had to understand the reason for it. The next step in examine the child was to evaluate the pupillary reflexes in both the eyes and they seemed to be brisk and normal. This indicated to me that there was unlikely to be a problem with one of the eyes’ nerves (optic nerves). After this, I dilated the child’s pupils with an eyedrop to look for presence of cataract and any pathology in the retina or nerve. I found all these to be normal. I understood that the cause for vision loss was likely related to the brain problem (encephalopathy). One last thing that we checked before completing the examination was the child’s refraction (or power of the eye) by retinoscopy. To my surprise, I found that the child had a very high plus power, in the range of +10 in both eyes. This made me think that the child may possibly have an ametropic amblyopia (lazy eye). However, I knew at this stage that a normal eye of a 1 year old child can also be a power of upto +5 or+6 and that I have to repeat the retinoscopy examination under atropine cycloplgia to get the true power of this child. I then explained to the parents that the child needs another checkup after putting eye ointment atropine and that we may have to prescribe glasses. The parents were very worried and reluctant to the idea of giving glasses to such a small child. I made them understand that if the child does not wear glasses when the power is so high, the eyesight will be very poor and the eyes will develop amblyopia (become a lazy eye) which will be difficult to treat at a later age. I also made them realise that if the child sees better and nystagmus reduces, then the child will be more likely to interact with his environment and this will greatly benefit the mental development. After this, the parents agreed and came back to me after 1 week after having put atropine in the child’s eyes. This time when we performed the retinsocopy test, we found that the power of the child’s eyes was +12 Dioptre and I prescribed glasses of the same number. The parents had lots of questions such as how will we ensure that the child wears the glasses, what type of glasses to use, how will the glasses stay on the child’s face, what if the child breaks the glass etc. I answered each of these questions for them. I told them that it was their duty to make the child wear the glasses and as long as the child is wearing the glasses, there will be improvement in vision and for every few hours that the child will not be wearing glasses, there will be a delay in improvement. I told them that children’s spectacles are special and are made of light, relatively unbreakable materials and have a band to tie them at the back of the head. I asked them to get the lenses made of polycarbonate material so that the lenses do not break even if the child was to throw the glasses around or something was to hit the child’s face. Finally I advised them to try the glasses with an open mind and see the difference it will make to their child. Convinced but still a bit reluctant, the parents accepted my advice and made a pair of glasses for the child.

The child came back to me after 1 month of using the glasses. The parents told me that the child had initially been irritated and tried to remove the glasses the moment they were place on the face but with the parents’ perseverance and occasional force and distraction, the child had started using the glasses in everyday. The parents told me that they were surprised to see the child adaprt so quickly and so well to the glasses that now if they removed the glasses for any reason, the child cried. I emphasised to them that the spectacles were giving the child a better vision and so the child liked wearing them. This is in fact a lesson to be learnt: if the proper power of glasses is given, most children will adapt to them very well and actually better than adults.

We let the child continue to use the glasses regularly. Over the next 6 months, the nystagmus seemed to reduce and the child could fixate better and started to interact better with his surroundings. There was a steadier gaze and as the child was more and more stimulated by the environment, there was improvement in mental status too. This was an excellent example of how the correction of 1 sensory system led to overall improvement in development.

At the last follow up, the child was 4 years old, able to stand, walk and speak basic sentences. The power of glasses had reduced by 1 Dioptre and nystagmus was significantly better.

In conclusion, this case demonstrates the need to evaluate all sensory systems when dealing with a child with developmental delay. It also highlights the need to optimise the sensory inputs to achieve better overall development. On the ocular rehabilitation front, it highlights the need for proper refraction, early prescription of glasses and need to counsel parents to ensure acceptability of spectacles.

I was referred a patient by a senior from New Delhi and when I examined the lady, I understood that this was no straight forward situation. It was a young woman in her early 20’s who had just delivered a healthy baby girl. Unfortunately for her, during the delivery she had a bleed in the brain and that left her with a left eye abducens nerve paralysis (Lateral rectus muscle paralysis) and a left gaze palsy. Her eyes would not move to the left side at all and the left eye was deviated inwards (convergent squint). There was a squint and she was having a double vision. She came to me after about 6 months after the brain haemorrhage and had shown little recovery during this period. I evaluated her and found that there was need to do surgery to correct her squint and help her get rid of the double vision because she was extremely distressed by it.

I performed a surgery in the left eye called a split vertical rectus transposition procedure where I augmented the force of the paralyzed lateral rectus muscle by shifting two vertical rectus muscles to the insertion of the lateral; rectus muscle after splitting them into half. In addition, I had to put two special sutures called the Foster sutures to ensure proper direction of force of the split vertical rectus muscles. I also weakened the left medial rectus muscle by a recesssion procedure. After the squint surgery, the eyes became straight and the squint disappeared. Surprisingly, there was some improvement in the eyemovements and gaze palsy also.

Now after 2 years of her surgery, she does not suffer from double vision and the squint is completely corrected. She tells me that she really enjoys playing with her 2.5 year old daughter and is happy her eye problem is over.

I am often asked by parents about why more and more children are needing glasses? Is there something they can do to prevent this? In this blog, I will address some of these concerns and will shed light on the growing burden of refractive errors.

Refractive error refers to weak eyes which need optical correction in the form of spectacles for achieving clear vision. Refractive error can be of many forms, namely hypermetropia (farsightedness) where the eye is smaller and less powerful than normal and requires plus powered glasses, myopia (shortsightedness) which occurs in those eyes which are a little longer than normal and more powerful requiring minus powered glasses and astigmatism where the shape of the cornea or lens is not spherical/round and a cylindrical lens is required for a clear vision. The commonest form among these is myopia and it is on the rise.

Myopia is a very common cause of visual disability throughout the world. It is usually diagnosed in early school years when children face difficulty in reading from the blackboard. Since near vision is normal in myopia, and prior to schooling most work done by the child involves large objects at a close distance, mild to moderate myopia goes undiagnosed till about 5-6 years of age. School myopia commences around 5-15 years of age and tends to stabilize in the late teens. Of late, there have been reports of more and more number of children requiring glasses and this has led to speculation that myopia is on the rise. In fact parents and teachers of most schools the national capital region and around India have spotted a higher number of children sporting glasses

The prevalence of myopia varies by the country, age and race. The prevalence of myopia has been reported to be as high as 70-90% in some Asian populations with Taiwan reporting a myopic prevalence of 84% among 16-18 - year old high school students. In India, the early surveys conducted the 1970's showed a prevalence of 4.79% among the school children in Chandigarh. It was higher in urban population @6.9% in comparison to rural population @2.77%. In an urban population in New Delhi, 7.4% of school children were found to have myopia in 2001-2. In a more recent survey among New Delhi school children in the 5-15 years age group, prevalence of myopia has been noted to be 13.1% suggestive of a significant increase over the last 15 years. Similar increase in prevalence has been reported from various studies all across the country. So it seems definite that we are facing an epidemic of refractive errors and spectacle use among children in India is going to be common sight just as it in Singapore and Taiwan.

So, what is causing this increase in myopia? The risk of developing myopia is influenced by genetic predisposition along with environmental factors. Traditionally, it is well known that children of parents wearing glasses are more likely to wear glasses than those whose parents don’t have a refractive error. While this is true to an extent, it is not the only aspect and more often than not children with no family history of refractive errors are having to use glasses. An interesting concept in genetics is the phenomenon of anticipation whereby what happens in one generation at a certain age happens earlier in the next generation and even earlier in the next. This may hold true for myopia as well since children of myopic parents seem to get glasses at an earlierage as compared to the parents. Certain known risk factors include premature and low birth-weight, poor nutrition, tall height and oriental origin (Hong Kong, Taiwan, Japan, and Singapore). Interestingly myopia is more often among persons who are more educated, have a higher educational level of the parents, higher intelligence and better socio-economic status. Numerous theories have attributed near work to increase in size(length) of the eye causing myopia. These find proof in the fact that certain occupations, such as sewing, and carpet weaving that require a large amount of time spent in close-up work have workers with higher prevalence of myopia. In fact, the increase in number of myopic persons in progressive generations has been attributed to increasing near tasks such as working on computer, video games, and television watching. Probably this may be the reason why myopia is less prevalent in the rural areas as compared to the urban areas. Though, there are no studies from India, based on the data from other Asian countries, overemphasis on academic performance and paucity of structured outdoor activity in the schools may be a factor contributing to the high myopia incidence rates in the very young.

Is there anything you can do as parents to prevent myopia or reduce its progression? Yes and no. If the cause for myopia is a genetic one then not much can be done to prevent its occurrence. A good diet and increased outdoor far-distance activities may mitigate the disease but definitive evidence for this is lacking. Ophthalmologists and parents have tried using certain eye drops (diluted atropine) to reduce the progression of myopia and limited success has been achieved in some studies. However with respect to Indian eyes, no such evidence exists and it has been noted that discontinuation of this treatment has resulted in the same amount of myopia as would have occurred if these drops were not being used. As of now this is an experimental treatment. The one thing you can do as parents is to bring your child for an eye checkup prior to them joining school and annually after that in order catch myopia early and enable appropriate use of glasses.